complications of airway management - respiratory...

Complications of Airway Management

Paulette C Pacheco-Lopez MD, Lauren C Berkow MD,Alexander T Hillel MD, and Lee M Akst MD

IntroductionMethodsResults

Risk FactorsInjury by Anatomic SiteLate Complications of IntubationSpecial Considerations

Conclusion

Although endotracheal intubation is commonly performed in the hospital setting, it is not withoutrisk. In this article, we review the impact of endotracheal intubation on airway injury by describingthe acute and long-term sequelae of each of the most commonly injured anatomic sites along therespiratory tract, including the nasal cavity, oral cavity, oropharynx, larynx, and trachea. Injuriescovered include nasoseptal injury, tongue injury, dental injury, mucosal lacerations, vocal cordimmobility, and laryngotracheal stenosis, as well as tracheomalacia, tracheoinnominate, and tra-cheoesophageal fistulas. We discuss the proposed mechanisms of tissue damage that relate to eachand present their most common clinical manifestations, along with their respective diagnostic andmanagement options. This article also includes a review of complications of airway managementpertaining to video laryngoscopy and supraglottic airway devices. Finally, potential strategies toprevent intubation-associated injuries are outlined. Key words: intubation; airway complications;subglottic stenosis; vocal cord injury [Respir Care 2014;59(6):1006–1021. © 2014 Daedalus Enterprises]

Introduction

The establishment of an adequate airway is integral tomanaging patients both in the elective operating room set-ting and in the emergent nonoperating room setting. En-dotracheal intubation is a basic skill performed daily by

health care professionals throughout the world and is arelatively safe maneuver. However, endotracheal intuba-tion is not risk-free, and its complications are well de-scribed in the literature. These can range from minor softtissue injuries to severe, long-term, life-threatening airwaycomplications.

The incidence of airway injury caused by endotrachealintubation ranges from 0.5 to 7%.1 Such injuries can occurat the initiation of intubation or can develop as a result ofprolonged intubation. According to a closed-claims anal-ysis by Domino et al.2 6% of claims against anesthesiol-ogy providers were for airway injury, with the larynx be-ing the most common site of injury, followed by the pharynxand the esophagus. Data from England documented byCook et al3 demonstrate a similar percentage of claimsrelated to airway management (8%). Beyond medicolegalissues, intubation-related injury is also a significant finan-cial burden. Patients with intubation-related injuries in-creased hospital costs by 20%, and stay was 1 d longerthan it was for matched patients without intubation injury.

Drs Pacheco-Lopez, Hillel, and Akst are affiliated with the Department ofOtolaryngology, and Dr Berkow is affiliated with the Department of Anes-thesia, Johns Hopkins University School of Medicine, Baltimore, Maryland.

Dr Berkow presented a version of this paper at the 52nd RESPIRATORY

CARE Journal Conference, “Adult Artificial Airways and Airway Ad-juncts,” held June 14 and 15, 2013, in St Petersburg, Florida.

The authors have disclosed no conflicts of interest.

Correspondence: Lauren C Berkow MD, Department of Anesthesia, JohnsHopkins University School of Medicine, Phipps 404, 600 North WolfeStreet, Baltimore, MD 21287. E-mail: [email protected].

DOI: 10.4187/respcare.02884

1006 RESPIRATORY CARE • JUNE 2014 VOL 59 NO 6

In addition, repeated admissions were more frequent in theinjured cohort.4

This review article will discuss several types of airwaycomplications from endotracheal intubation. Some inju-ries, such as soft tissue hematomas, lacerations, and ary-tenoid dislocation, may result from the initial act of intu-bation. Other injuries, such as laryngotracheal stenosis andvocal fold paralysis, may result from tissue-endotrachealtube (ETT) interactions, even if intubation was performedwithout direct tissue trauma. We will review both catego-ries of injury and focus on risk factors, pathogenesis, pre-sentation, and management of some of the most commonlyseen complications.

Methods

We carried out a systematic search of the PubMed da-tabase. A broad search was used so as to augment thecitations of peer-reviewed journals regarding airway com-plications in endotracheal intubation. The Medical SubjectHeadings used in the search were: airway, oral cavity,oropharyngeal, laryngeal, subglottic, and tracheal compli-cations AND endotracheal or nasotracheal intubation,GlideScope, or laryngeal airway mask. The searches wererepeated in combination with epidemiology, pathophysi-ology, and treatment. In addition, we carried out manualsearches within the references of pertinent articles. Thesearch was limited to articles published in the Englishlanguage, but no date restrictions were applied.

Results

Risk Factors

In attempts to diminish morbidity and to improve pa-tient care, many have sought to define the risk factors forairway injury during endotracheal intubation. As might beexpected, intubations categorized as difficult pose a higherrisk of injury than do those that are not difficult. Never-theless, 39% of airway injuries described in a closed-claimsanalysis were associated with difficult emergent intuba-tions, even though the incidence of difficult intubationamong patients undergoing elective surgery has been re-ported to be only 5.8%.5 However, the incidence of diffi-cult intubation is higher in the emergent setting comparedwith elective procedures (8–12 vs 6%).1 Emergent airwaymanagement often requires physicians to intervene ur-gently, without adequate time to obtain a thorough patienthistory. Patients are also more likely to be hemodynami-cally unstable, a condition that might contribute to thecomplexity of intubation in this setting.

The skill level of the provider who performs the intu-bation has also been studied as a potential risk factor forairway complications. Skill level inversely correlates with

number of attempts at laryngoscopy, with higher skill lev-els correlating with fewer attempts, and repeated laryngos-copy attempts may lead to tissue trauma, edema, and bleed-ing.1 Indeed, complications increase 7-fold after the secondand third laryngoscopy attempts.6 Patients of junior resi-dents have complication rates ranging from 4 to 9% inemergent situations, whereas those of senior residents haveonly a 2.3% complication rate.1,7-9 Attending supervisionduring emergent intubation also appears to lower compli-cation rates significantly (6 vs 21%, P � .001).8 Schmidtet al8 stated that attending supervision of emergent intu-bations occurred more frequently in the ICU than in thewards and that patients in the ICU were more likely toreceive muscle relaxants for intubation. The role of attend-ing supervision has been the source of much debate be-cause the mere presence of a second anesthesia provider,regardless of experience level, may facilitate intubation.10

Therefore, it is unclear whether the decrease in complica-tion rate results from the additional help provided by asecond anesthesiologist or relates specifically to the levelof training of the provider performing the intubation.

Patient factors also influence the degree and severity ofairway complications after endotracheal intubation. Somesystemic conditions can predispose patients to develop ma-jor complications from the physiologic insult of intuba-tion. These factors are being investigated, but it remainsunclear why some patients develop long-term sequelae,whereas others exposed to the same mechanisms of injurydo not. There appears to be a trend toward a higher inci-dence of airway injury in patients with diabetes mellitus,hypertension, hypotension, heart disease, kidney or liverfailure, and malnutrition.11,12 It is believed that these dis-ease states may lead to poor tissue perfusion, with impli-cations for wound healing, necrosis, and ulceration.12,13

Likewise, laryngopharyngeal reflux has also been impli-cated as a risk factor.14 Laryngopharyngeal reflux maycause airway injury in critically ill patients because gastricacid can spill over the larynx and expose tissues to pepsin,exacerbating local injury, delaying wound healing, andpredisposing the patient to infection.12

The roles that patient age and gender might play incomplications of endotracheal intubation are unclear, withstudies arguing both for and against their impact. Kikuraet al11 found that patients who were � 50 y old had 3 timesthe risk of younger patients for developing vocal cordparalysis. Female gender also has been suggested as a riskfactor for developing postextubation laryngeal edema andsubglottic stenosis.15-17 It has been speculated that the la-ryngotracheal mucosa in men may be more resilient totrauma than that in women and that the dimensions of thelarynx and trachea are smaller in women than in men,making them more prone to injury, especially if an inad-equately sized tube is used.18,19 Other studies have foundno correlation between laryngeal injury or vocal fold im-

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mobility after controlling for age, gender, height, andweight.20

Obesity as a predictor of the difficult airway has beenwell studied, and specific challenges are known to be in-herent to intubation of obese patients.21-23 Obese patientsmay have crowding and distortion of the oropharynx, lim-ited neck extension, a higher incidence of comorbid con-ditions, and a lower tolerance for apnea and tissue hyp-oxia.21,23,24 Holmberg et al21 observed that class I/II obesity(body mass index � 30 kg/m2 and � 40 kg/m2) in patientswas not associated with difficult intubation, whereas pa-tients with body mass index � 40 kg/m2 had higher ratesof difficult intubation. Despite the relationship betweenobesity and difficult intubation, however, it remains un-clear whether obesity is a risk factor for complicationsfrom intubation. Colton House et al20 found that weightdoes not appear to have a significant correlation with theincidence of laryngeal injury. Likewise, Dargin et al25 con-cluded that body mass index was not predictive of postin-tubation complications. Interestingly, they also found thatobesity, but not morbid obesity, predicted difficult intuba-tion. Currently, the relationships between obesity, difficultintubation, and intubation-related injury remain uncertain.

Injury by Anatomic Site

Nasal Cavity. Nasotracheal intubation is a common al-ternative to orotracheal intubation in patients for whomsurgical access to the oral cavity is necessary, such as insome head-and-neck, otolaryngology, or maxillofacial sur-gery cases. Nasotracheal intubation may also be the pre-ferred method of intubation in patients with trismus. Theincidence of epistaxis during nasotracheal intubation rangesfrom 29 to 96%.26-28 Epistaxis may result from soft tissueinjury, such as mucosal abrasions, tears, or lacerations.Self-limited epistaxis is the most common presentation ofminor soft tissue injury to the nasal mucosa. More seriousinjuries should be considered if blood pools in the oralcavity. Life-threatening blood loss from epistaxis has alsobeen reported.29 If blood remains trapped deep in mucosalsurfaces within the nose, hematomas may result, leading toconcern for devascularization of underlying cartilage andsubsequent structural deformity.

Investigators have compared intubation of the right andleft nostrils to determine whether laterality poses a differ-ence in complication rates. Coe and Human30 found nosignificant difference in bleeding based on nostril side.Sanuki et al31 documented the left nostril as being moreprone to severe epistaxis (22% (left) vs 0% (right), P � .02).The left side might be injured more frequently because thebeveled tip of the ETT faces the left side and impacts themore vascular mucosa of the turbinates.32 The most com-mon injury is bruising at the septum or inferior turbi-nate.26,27 However, forceful nasotracheal intubations can

also cause inadvertent injury to the lateral nasal wall, caus-ing accidental avulsion of the turbinates33-35 and posteriorpharyngeal lacerations.36,37

Although generally considered a temporary mode ofintubation, some patients require prolonged intubation viathe nasotracheal route. Long-term injury can be related tomalpositioning of the tube against the nasal alae, causingischemia, ulceration, and ultimately pressure necrosis ofthe alar tissue. In addition, prolonged nasotracheal intuba-tion has been associated with sinusitis, which can developwhen the ETT obstructs maxillary sinus drainage.38 How-ever, other studies have documented no significant differ-ence in the incidence of sinusitis between patients whohave prolonged orotracheal intubation and those who haveprolonged nasotracheal intubation.39

Preoperative nasal endoscopy and digital manipulationmay be used to determine the most patent nostril in aneffort to limit complications from nasotracheal intubation.In addition, ample use of lubricants; nasal decongestionwith cocaine, epinephrine, or oxymetazoline; and warmingof the tube may be used to facilitate tube passage.40,41 Themanagement of nasotracheal injury depends on its sever-ity. Mucosal abrasions, tears, and hematomas usually re-solve with conservative management, such as nasal hu-midification and nasal pressure. Large septal hematomascan cause concern for potential septal perforation, as dis-section of the mucoperichondrium from the underlyingcartilage may compromise vascular supply. If large septalhematomas are identified, otolaryngology consultation formanagement and drainage is recommended.42,43 Otherforms of injury, such as turbinate avulsion, might alsorequire otolaryngology evaluation to determine the needfor nasal packing or cauterization of the mucosa if bleed-ing persists. Pharyngeal lacerations may heal without sig-nificant sequelae, but in these cases, one should watchvigilantly for the development of retropharyngeal hema-tomas or abscesses that may lead to airway compromise.Pressure sores of the nasal alae may be managed with localcare unless significant necrosis has led to loss of tissue andcosmetic deformity. Such defects require plastic recon-struction.

Oral Cavity and Oropharynx. Dental injury during la-ryngoscopy is one of the most common complaints againstanesthesiologists.44,45 These types of injuries are often dueto pressure on the maxillary incisors, which anesthesiolo-gists sometimes use as a fulcrum for the laryngoscopewhile attempting to visualize the larynx. Laryngoscopymay also cause inadvertent soft tissue injury to the lips,buccal mucosa, floor of mouth, palate, and tongue. Theseinjuries can also be caused by the insertion of ETTs, oro-gastric tubes, temperature probes, and oral airways. Themechanism of injury is direct tissue trauma from the of-fending medical device. Oral cavity injury should be sus-



pected in the presence of mucosal discoloration and he-matoma formation, blood-tinged secretions, or oozing ofblood from scraped or lacerated surfaces during suction-ing. The severity of injury ranges from minor hematomasand mucosal lacerations that heal spontaneously to largersoft tissue defects that may require primary repair withsuture. Mediastinitis and internal carotid thrombosis havealso been described after oropharyngeal perforations, butthese are exceedingly rare.46,47

Larynx

Hoarseness. Ninety-seven percent of intubations, evenfor very brief periods, may lead to some form of laryngealinjury.12,48,49 Injuries may include vocal cord erythema,ulcers, granulomas, and, less commonly, vocal cord im-mobility.48 After being extubated, many patients have tran-sient complaints of vocal fatigue, dysphagia, sore throat,hoarseness, throat clearing, and aspiration. Hamdan et al50

studied the short-term effects of intubation on voice andfound that the most important variables associated with anincrease in vocal symptoms were mean cuff pressure andvolume. Patients with persistent vocal fatigue had highermean cuff volumes than did patients without that symp-tom, and persistent throat clearing was more prevalent inpatients with higher mean cuff pressures.50 However, Ham-dan et al50 also documented that most of these symptomsresolved within 24 h. When symptoms persist or progress,the presence of more serious injuries, such as vocal foldlacerations, hematomas, or avulsion, must be consideredbecause these injuries usually take longer to heal and couldpotentially lead to poor voice outcomes, prolonged voiceproblems, and vocal fold scarring.51 In a survey of patientsregarding postintubation dysphonia, 49% of patients statedthat they had vocal difficulty on the day of surgery, but thesymptoms improved over time, with 29, 11, and 0.8%stating that dysphonia was present on postoperative days1, 3, and 7, respectively.52 It is estimated that 1% of pa-tients may continue to experience dysphonia related tochronic injury of the vocal folds after acute and subacutehealing are complete.11

Vocal Cord Paralysis. Patients may develop vocal foldparalysis secondary to short-term or long-term intubation.12

This is an exceedingly rare injury and is thought to occurin only 0.033–0.07% of intubations.11,53 When viewed asa proportion of cases of vocal cord paralysis rather than asa percentage of intubations, vocal fold paralysis related tointubation injury seems more common. Intubation is esti-mated to be the cause of paralysis in 4–7.5% of cases ofunilateral vocal fold immobility and 9–25% of cases ofbilateral vocal fold immobility.54,55 To put these numbersinto perspective, iatrogenic injury to the recurrent laryn-geal nerves during surgery (such as carotid endarterecto-

mies, anterior approaches to the cervical spine, and thyroidsurgeries) accounts for the largest proportion of vocal foldimmobility cases (23.9–56%).54

Several theories have been put forth to explain the patho-genesis of recurrent laryngeal nerve paralysis after endotra-cheal intubation. The recurrent laryngeal nerve runs in thetrachea-esophageal groove lateral to the cricoid cartilage; itsinternal branch then enters the larynx between the cricoid andthyroid cartilages near the cricoarytenoid joint. Its endolaryn-geal segment is especially vulnerable to compression betweenan ETT cuff and the internal thyroid lamina, particularly ifthe cuff sits too high and if the cuff pressures exceed capillaryperfusion pressure. This compression may compromise vas-cularity and result in nerve dysfunction.53,56,57 Awareness ofmaintaining appropriate cuff pressures is widespread. How-ever, recent reports have documented that cuff pressures mayincrease from baseline values when cervical retractors arepositioned for exposure during anterior cervical spine sur-gery.58,59 In addition, cadaver studies performed by Kriskov-ich et al59 confirmed that cervical retractors may displace thelarynx against the shaft of the ETT with impingement on thevulnerable intralaryngeal segment of the recurrent laryngealnerve. The authors proposed that deflating the cuff after re-tractors have been positioned enables the tube to migrateinferiorly and diminishes the incidence of paralysis.59 How-ever, a similar study by Audu et al60 documented that al-though cuff deflation/inflation decreased ETT cuff pressure,it did not reduce the incidence of vocal fold immobility(15.4 vs 14.5%). Stretching of the nerve during tube manip-ulation or intubation has also been proposed as a mechanismof injury.61

Symptoms of vocal fold immobility include acute onsetof weak breathy voice and increased vocal effort. Occa-sionally, dysphonia related to vocal fold immobility is alsoassociated with dysphagia and increased aspiration risk.When unilateral vocal fold immobility is suspected, oto-laryngology examination with visualization of the larynxcan confirm the diagnosis. Physical examination shouldinclude a complete head-and-neck exam and assessmentfor other cranial nerve injuries. Flexible or mirror laryn-goscopy is also essential for assessment of mobility. Aparalyzed vocal fold is usually found in the paramedianposition (75%) and is less often in the lateral (13%) ormidline (11.3%) position (Fig. 1).62 The position of paral-ysis was once believed to depend on whether the superiorlaryngeal nerve was injured, causing the vocal fold to liein a more lateral position. However, subsequent studieshave shown that the superior laryngeal nerve and hencecricothyroid muscle function do not predict vocal cordposition. Rather, the position of paralysis depends on thedegree of reinnervation and synkinesis present.63-65 Whensome adductor motion is present on laryngoscopy, it shouldnot be confused with mobility. Instead, this motion may becaused by contralateral innervation of the interarytenoid



muscle, which contributes to vocal cord adduction bilat-erally.65 Atrophy and bowing of the paralyzed cord andanterior rotation of the arytenoid are also common find-ings. Stroboscopy may show evidence of height mismatch-ing and a diminished, asymmetric, or absent mucosal wavewhen the vocal cord lies in the paramedian or lateral po-sition.66 This position significantly compromises glottalcompetence and phonation, thus worsening patient symp-toms. Left immobility is more common than right immo-bility, perhaps because most intubations are performedfrom the right side using the right hand. Therefore, thetube tends to rest toward the right side proximally, andtoward the left side distally.12,20,54,55

Patients may recover spontaneously when recurrent laryn-geal nerve continuity has been preserved. If no motion isappreciated within 6–12 months and/or electromyographyshows signs of denervation, recovery is unlikely. Midline

unilateral paralysis rarely requires intervention. However, pa-tients who have glottic insufficiency related to a paramedianor lateral position of the paralyzed vocal fold may benefitfrom medialization of the immobile vocal fold to the midlineso that glottic closure is improved. Techniques for medial-ization include vocal fold injection, laryngeal framework sur-gery, and arytenoid adduction procedures; these techniquescan re-establish glottal competence, strengthen the voice, andimprove swallowing safety. If it is unknown whether paral-ysis is temporary or permanent, temporary injection augmen-tations can support voice and swallowing while the patientawaits potential recovery. Although studies are sparse, lim-ited information suggests that 35% of patients with unilateralvocal fold paralysis will experience recovery without needfor subsequent intervention.67

Arytenoid Dislocation and Subluxation. Unilateralvocal cord immobility related to intubation can also occuras a result of mechanical fixation of the cricoarytenoidjoint, rather than as a consequence of recurrent laryngealnerve injury. As it relates to intubation, the possibility thatmechanical loss of vocal fold motion may be caused bydirect trauma to the arytenoid cartilage itself is controver-sial. In this context, arytenoid dislocation refers to com-plete loss of contact between the cricoid and arytenoidcartilages, and subluxation refers to only partial loss ofcontact.68 Vocal fold immobility secondary to arytenoiddislocation is considered rare, and some specialists donot think that true arytenoid dislocation is possible on ananatomic basis.69 Unfortunately, true incidence rates ofarytenoid dislocation or subluxation are unclear becauseunilateral vocal fold immobility may be attributed to neu-rogenic vocal fold paralysis rather than mechanical fixa-tion. Physical examination can sometimes offer insightinto the differential diagnosis between neurogenic paraly-sis and joint fixation: faint twitches of motion suggest amobile joint, whereas complete immobility and a malro-tated arytenoid might instead suggest mechanical issues,such as arytenoid subluxation. Electromyography and jointpalpation with the patient under general anesthesia canalso be used to distinguish between mechanical and neu-rogenic causes of vocal fold immobility.

Using histologic studies, Paulsen et al70 found that thecricoarytenoid joint contains large synovial folds that arevulnerable to trauma by forceful intubation. Trauma tothese folds can potentially lead to hemarthrosis, joint ad-hesion, and fixation of the arytenoid in an abnormal po-sition.70 The most common cause of arytenoid dislocationand subluxation is thought to be intubation trauma, withposterior dislocation being more common than anteriordislocation.71 The proposed mechanism of injury for an-terior arytenoid dislocation is described in the literature asdirect forward pressure on the posterior arytenoid, eitherby the laryngoscope used for intubation or by the ETT

Fig. 1. A: Right vocal cord paralysis, abduction. Note bowing andloss of tone on the right versus the left side. There is asymmetry inthe position of the arytenoids during full abduction. The right ar-ytenoid is anteriorly rotated, while the left moves posterolaterallyduring inspiration. B: Right vocal cord paralysis, adduction. Notebowing and loss of tone of the right vocal cord. There is a glottalgap on full adduction, as well as left compensatory false vocal foldcompression that obstructs the view of the left true vocal cord.



itself pushing the arytenoid anteriorly off the cricoid facet.Posterior dislocation is believed to occur during extuba-tion, perhaps during removal of an incompletely deflatedcuff.72 Despite the alleged mechanisms of possible aryte-noid dislocation, the very existence of the entity remainscontroversial. Some authors suggest that traumatic dislo-cation is impossible. Attempts at purposeful dislocation incadaveric larynges have been unsuccessful because thelaryngeal musculature preserves the integrity of the saddlejoint relationship of the cricoid and arytenoid cartilages.69,73

The clinical symptoms of patients with cricoarytenoiddislocation are similar to those of patients with true vocalcord paralysis, with hoarseness, breathiness, and vocal fa-tigue being the most common. Direct laryngoscopy of pa-tients under general anesthesia can be an important step tohelp differentiate between arytenoid fixation or dislocationand neurogenic paralysis, as joint palpation allows for as-sessment of passive joint mobility.65 The same otolaryn-gologic direct laryngoscopy that allows for arytenoid pal-pation to differentiate between neurogenic paralysis andmechanical fixation also provides a therapeutic option forpatients with suspected dislocation, as endoscopic reduc-tion can be performed immediately upon diagnosis. De-spite the controversial nature of the very existence of truearytenoid dislocation, recent reports document that closedreductions can provide satisfactory improvements in voiceeven after late surgical intervention.62,71,74

Late Complications of Intubation

Laryngotracheal Stenosis. In contrast to many of theinjuries discussed thus far, which occur acutely duringintubation or after a short period of intubation, laryngo-tracheal stenosis can be a long-term consequence of pro-longed intubation. In fact, the most common cause of adultlaryngotracheal stenosis is endotracheal intubation.75,76 Theduration of intubation has been found to correlate signif-icantly with the incidence of laryngeal pathologies, includ-ing the development of subglottic edema and narrowingwhen intubation time exceeds 7 d.16,77 However, ColtonHouse et al20 demonstrated no significant difference in thedevelopment of subglottic edema regardless of duration ofintubation or tube size. The presence of comorbidities,such as diabetes mellitus, gastroesophageal reflux, and im-munosuppression, have also been shown to predispose pa-tients to develop stenosis.17,20,78,79 Therefore, this popula-tion would perhaps benefit from early tracheotomy.78

The reported historical incidence of laryngotracheal ste-nosis after endotracheal intubation ranges from 1 to21%,76,80 but it is hoped that increasing knowledge abouthow to limit airway injury from prolonged intubation willreduce these rates. Inflammatory changes in the posteriorglottis can be seen as early as 2–5 d after intubation.77 Awidely accepted mechanism of injury is localized tissueischemia that occurs when the pressure exerted by the ETT

Fig. 2. Diagram chart of possible outcomes of ulceration, namely, intubation granuloma, interarytenoid adhesion, and healed fibrous nodule.From Reference 12, with permission.



exceeds tissue capillary pressure. The excessive pressurecan lead to vascular damage and formation of edema, gran-ulation, and ulcers.12 The most common sites at the levelof the larynx are the posterior glottis and interarytenoidregions, where the ETT rests. The progression to scar tis-sue has been described by Benjamin and Holinger12 as acontinuum of disease that begins with localized tissue isch-emia that results from compression by the ETT and pro-gresses to necrosis and ulcer formation, especially at areasof exposed perichondrium, such as the vocal processes(Fig. 2). The reparative process continues with the forma-tion of granulation tissue, a hallmark of wound healing,which involves neovascularization as well as proliferationof inflammatory cells and fibroblasts (Fig. 3). As the gran-ulomas mature and proliferate, deposition of collagen even-tually leads to scar formation and tissue contracture.12 Ste-nosis may occur at any subsite where tissues are in contactwith the ETT or cuff, namely the posterior glottis, sub-glottis, and proximal trachea (Figs. 4 and 5). Injuries mayspan more than one level in 25% of cases, as documentedby Anand et al.80

Scarring and fibrosis in the interarytenoid or posteriorglottic region impair adequate vocal cord abduction bilat-erally and may resemble bilateral vocal cord paralysis (Fig.5). Failure to adequately abduct with inspiration can com-

promise the airway and lead to dyspnea, stridor, or respi-ratory failure.81 As the scar matures in the weeks afterextubation, the posterior glottis becomes progressively nar-rower, resulting in the development of exertional dyspneawith inspiratory stridor. If an office laryngeal examinationconfirms that vocal cord abduction is reduced or absent,further laryngeal examination of the patient under anes-

Fig. 3. A: Operative view of a normal glottis. B: Bilateral vocalprocess granulomas.

Fig. 4. Posterior glottic stenosis.

Fig. 5. Postintubation tracheal stenosis. A: Views from above thevocal cords. B: Views from below the vocal cords.



thesia may be warranted to examine the posterior glottis.Palpation of the bilateral arytenoids can be used to differ-entiate posterior glottic scarring from neurogenic paraly-sis, and endoscopic examination of the subglottis and tra-chea can help to rule out synchronous lesions. In addition,laryngeal electromyography may aid in differentiating neu-rogenic and mechanical sources of immobility.

The anesthesiologist and the otolaryngologist should dis-cuss airway management of a patient before beginningoperative treatment of laryngotracheal stenosis. Routineintubation of a patient with airway stenosis may or maynot be possible, and safe operative intervention requiresthat contingency plans be discussed in advance. The ste-notic site can limit tube passage, causing trauma to themucosa, promoting edema and swelling of the tissues, andpotentially leading to complete airway obstruction. Man-aging the airway in cases of severe stenosis may requirethat a tracheotomy be performed with the patient awakeand under local anesthesia. After the tracheotomy, venti-lation can be provided via the tracheal stoma, and thelarynx can be evaluated without the ETT hindering visu-alization or obstructing the surgical site. However, patientswith a stable airway may benefit from less invasive mo-dalities, such as jet ventilation, if the stenosis allows foradequate exhalation without air trapping. Intermittent ven-tilation through rigid bronchoscopy is also an alternative,although the frequent insertion and removal of the scopethroughout the surgical procedure may be cumbersome.

During endoscopic evaluation of posterior glottic steno-sis, joint mobility should be assessed by palpation. If thejoint is mobile, but scar tissue causes immobility of theposterior commissure, the scar tissue can be divided withposterior glottic lysis to help re-establish mobility. Coldinstrumentation or a laser can be used for microsurgicalscar excision. However, restenosis can occur if raw sur-faces appose during healing. Rotation of mucosal flapsinto the exposed surfaces may prevent adhesion formationand restenosis.82,83 If the glottic scar does not respond toconservative lysis of the posterior commissure, then uni-lateral cordotomy and partial arytenoidectomy may helpimprove glottic airway patency, although at the cost ofpossible breathy dysphonia.

The management of subglottic and tracheal stenosis de-pends largely on the characteristics of the stenotic regionas seen by endoscopy. It is important to measure the dis-tance from the glottis to the onset of the stenotic segment,the length of the stenosis, and the distance from the distalportion of the stenosis to the tracheal stoma (if the patienthas already had a tracheotomy). Treatment includes endo-scopic procedures, such as serial dilations with rigid bron-choscopy, balloon dilations, and laser resection. Historicalsuccess rates of endoscopic procedures range between 44and 68%.84-86 However, these procedures are usually mosteffective in the treatment of thin web-like lesions that are

no longer than 2 cm. Mitomycin C, an antineoplastic agentthat inhibits fibroblast proliferation, has been shown to bean effective adjuvant in preventing restenosis,87 althoughmany reports are anecdotal, and the literature lacks con-trolled studies. In addition, the use of T-tube stenting canbe considered if multiple endoscopic treatments have failedto correct the stenosis. External procedures, such as laryn-gotracheal reconstruction with anterior and/or posterior car-tilage grafting and cricotracheal/tracheal resection withanastomosis, are possible options for stenoses longer than2 cm or for patients in whom multiple endoscopic proce-dures have failed.

Structural Changes to the Trachea. The most commoncauses of acquired tracheomalacia are cuffed endotrachealor tracheotomy tubes.88 The pathophysiology of tracheo-malacia has been described as a combination of pressurenecrosis secondary to elevated cuff pressures, mechanicalerosion due to movement of the tube, chronic inflamma-tion, and infection contributing to thinning and destructionof the tracheal cartilages.88,89 Loss of this cartilaginoussupport causes weakening of the tracheal wall, followedby collapse and airway obstruction during respiration. Clin-ical manifestations can range from mild dyspnea, chroniccough, and wheezing to more serious airway events, suchas stridor, airway compromise, and eventual respiratoryfailure.90 Management of tracheomalacia includes trache-otomy to bypass the malacic site,91 intraluminal stenting,90

external stabilization with stenting,92 and surgical resec-tion of the malacic segment with end-to-end anastomosis.

Tracheotomy and prolonged intubation may lead to an-other rare yet devastating complication: tracheoinnomi-nate artery fistula. The pathophysiologic mechanism in-volves pressure necrosis of the tube tip or cuff withsubsequent erosion of the anterior tracheal wall.93 Thiserosion can cause a fistulous communication between thetrachea and the innominate artery as it passes anteriorlyacross the trachea. The clinical presentation of tracheoin-nominate artery fistula is classically described as a sentinelbleed followed by massive hemoptysis.93,94 Its diagnosisrequires a high index of clinical suspicion because otherdiagnostic modalities, such as angiography, can delay man-agement and lead to death. An immediate intervention thatcan be used to stop the bleeding is hyperinflation of thetracheotomy cuff. If this fails to control bleeding, the tra-cheotomy tube should be replaced by an ETT through thetracheostoma so that the cuff can be inflated distal to thebleeding site; digital pressure with a finger inserted throughthe stoma into the airway can help compress the anteriortracheal wall and innominate artery against the sternum.This compression may slow acute bleeding in 90% ofpatients94 and allow time for emergent transport to theoperating room, where definitive management can takeplace. Tracheoinnominate artery fistula is a life-threaten-



ing complication with a published survival rate of only14%; the key to potential survival is immediate surgery.95

A tracheoesophageal fistula may also develop as a resultof prolonged endotracheal intubation or tracheotomy. Themechanism of injury is similar to that of tracheomalaciaand tracheoinnominate fistula, in which elevated cuff pres-sures, necrosis of the mucosa, and subsequent erosion ofthe tracheoesophageal wall can lead to a fistulous tractbetween the posterior wall of the trachea and the anteriorwall of the esophagus. This complication is more com-monly identified in the ICU setting when patients are stillcritically ill and dependent upon prolonged mechanicalventilation. Risk factors include diabetes, infection, andthe presence of a nasogastric tube.96,97 Clinically, a tra-cheoesophageal fistula can be identified when food con-tent is suctioned from the ETT or if the patient presentswith coughing during feeding, recurrent aspiration pneu-monia, positive cuff leak, or gastric distention.98 Diagnosiscan be confirmed with radiology studies, such as an esopha-gram or computed tomography scan, or instead confirmedwith esophagoscopy and bronchoscopy. Once the diagno-

sis is established, surgical repair is required because spon-taneous closure is rare.97,99

Special Considerations

Video Laryngoscopy Injuries. Since the introduction ofthe video laryngoscope in 2002, a series of case reportshave been published that document the complications en-countered with its use (Table 1).100-112 The most commoncomplication is injury to the soft palate, although injuriesto the teeth, larynx, tongue, and retromolar trigone havealso been described.110-112 The oropharynx is specificallyat risk of injury because the video laryngoscope causes thetonsillar pillars to elevate and stretch anteriorly, makingthem more prone to injury as the tube is being advanced.102

The mechanism of injury with the video laryngoscope dif-fers from that with traditional intubation. The soft tissuedamage in traditional laryngoscopy is caused mainly byinsertion of the laryngoscope, but soft tissue injury withthe video laryngoscope is caused by insertion of the ETTitself, as it is often maneuvered blindly into and through

Table 1. Video Laryngoscope Complications: Summary of Case Reports

Injury Type Mechanism Repair Reference

Palatoglossal arch Blind insertion of styleted tube into pharynx No Hsu et al100

Rigid styleted tube, focusing on monitor and not oralcavity

No Hirabayashi101

Palatopharyngeal arch Styleted tube inserted laterally and blindly rotatedanteriorly to bring into view

No Leong et al102

NR Yes, suture Cooper103

NR Yes, cautery Cooper103

Soft palate Rigid styleted tube, focusing on monitor and not on oralcavity

No Vincent et al104

Styleted tube inserted laterally and blindly rotatedanteriorly to bring into view

No Cross et al108

McGrath video laryngoscope, styleted tube, blind spotwhile focusing on monitor and not oral cavity

Yes, suture Williams and Ball105

Rigid styleted tube, focusing on monitor and not on oralcavity

No Hsu et al106

Rigid styleted tube, focusing on monitor and not on oralcavity

Yes, suture Chin et al107

Rigid styleted tube, focusing on monitor and not on oralcavity; tube inserted laterally and blindly rotatedanteriorly to bring into view

No Cross et al108

Tonsillar pillar Blind intubation while focusing on monitor; standardtube, not rigid stylet as recommended by manufacturer

No Malik and Frogel109

Retromolar trigone, possible lingualnerve injury

Blind tube placement using rigid stylet No Magboul and Joel110

Base of tongue NR Unknown Dupanovic111

Dental (n � 2), vocal cord (n � 1),trachea (n � 1), hypopharynx (n � 1),tonsil (n � 1)

NR Unknown Aziz et al112

NR � not reported



the oral cavity and pharynx until it is finally in view at thevideo laryngoscope monitor. Injuries often occur becauseof the natural tendency of the intubator to focus on themonitor and not toward the oral cavity or oropharynx dur-ing tube insertion.103,105 In addition, Dupanovic111 de-scribed the GlideScope GVL’s (LoPro medical blade, Ve-rathon,Bothell,Washington) 2blind spots: one at its inferioraspect and the other at its lateral aspect. These precludedirect visualization of the ETT as it is being inserted by theoperator.

The proprietary stylet marketed with the GlideScope isdesigned to follow the curve of the video laryngoscope.This stylet is more rigid than a standard ETT stylet andmay increase the risk of soft tissue injury. Studies havedemonstrated that a standard ETT stylet is equally suc-cessful for intubation when used by novice and experi-enced operators.113,114

Management depends on the severity of soft tissue in-jury; mild lacerations can be managed conservatively,whereas more substantial injuries may benefit from hemo-stasis and primary repair. In a literature review by Leonget al,102 all 11 patients suffered injury to the soft palate,mainly the palatopharyngeal arch, the palatoglossal arch,and the anterior tonsillar pillar. However, only 4 of 11patients required otolaryngology intervention. Two patientsrequired sutures, and 2 patients required electrocautery tocontrol bleeding.103,107

To reduce the incidence of this complication, severalauthors have proposed different techniques of tube inser-tion: (1) always maintain the tip of the tube close andparallel to the blade until it is viewed in the monitor, (2)keep the tube in direct vision during placement and refrainfrom looking back to the monitor until the tip has passedout of direct vision, and (3) insert the tube in the midlinewith the proximal portion oriented to the right and thenrotate counterclockwise 90° to bring the tip intoview.102,103,111 Knowledge of these complications and thetechniques to prevent them is paramount in reducing pa-tient morbidity.

Several other video laryngoscopes have been introducedto the market recently. Though reports of injury with useof these other videoscopes are rare, it should be assumedthat the risk of injury is equivalent to that of the Glide-Scope, and similar precautions should be taken to preventinjury.

Supraglottic Airway Device Injuries. Introduced in1991, the laryngeal mask airway (LMA) was the first su-praglottic airway device created for use as an alternative toendotracheal intubation. Several supraglottic airway de-vices are now available and are currently used in manysettings. These devices can be used in the emergent settingwhen endotracheal intubation is unsuccessful and in thecontrolled operating room setting as a less invasive alter-

native to endotracheal intubation. Risks and complicationshave only recently been reported for the LMA, even thoughit is generally considered to be safer than endotrachealintubation.

Reported soft tissue injuries from the LMA includetongue ischemia,115 as well as both unilateral and bilateralrecurrent laryngeal,116,117 hypoglossal,118 and lingual119

nerve injuries. The proposed injurious mechanism is sim-ilar to that described with classic ETT injury: direct me-chanical compression of the nerve between the LMA cuffand the cricoid as it ascends at the apex of the pyriformfossa.116 The increase in cuff pressure is not necessarilycaused by manual overinflation. Instead, it has been pos-tulated that nitrous oxide from gas anesthesia diffuses intothe supraglottic airway device cuff and inadvertently in-creases cuff pressure.117 As this cuff pressure exceeds cap-illary perfusion pressure, the nerve may undergo neuro-praxic injury and manifest clinically as vocal cord paralysis,hemi-tongue paralysis, tongue anesthesia, etc.120

Most of these injuries are transient and will likely re-solve spontaneously. In a literature review, Endo et al117

reported that only 2 of 14 patients had permanent injuriesafter LMA use. To prevent neural damage, El Toukhy andTweedie119 listed a series of points: (1) select the appro-priate size for supraglottic airway devices; (2) avoid cuffpressures that exceed 60 cm H2O; (3) when using nitrousoxide, routinely measure cuff pressure every 30 min; (4)avoid extreme neck positions; and (5) have a low thresholdof suspicion for nerve damage.

Conclusion

Endotracheal intubation can be a safe, life-saving pro-cedure. Although rare, acute or chronic injuries can occurduring endotracheal intubation. Emergent and difficult in-tubations are significant risk factors for airway injury. Theskill level of the provider performing the intubation hasalso been studied, but results in the literature have beenconflicting. Likewise, the role of patient factors, such asage, gender, and obesity, and how they relate to compli-cations are still controversial. Soft tissue hematomas andlacerations may occur in the nasal and oral cavities, oro-pharynx, and larynx. These injuries are caused mostly bymishaps during laryngoscopy or tube insertion. Most ofthese injuries heal on their own without causing severesymptoms or permanent sequelae.

More serious injuries should be considered when symp-toms such as hoarseness, dysphagia, and breathing diffi-culties ensue or persist. In these cases, vocal cord paraly-sis, arytenoid dislocation, and laryngotracheal stenosis mustbe considered as possible etiologies. Such airway injuriesmay develop after prolonged intubation when laryngotra-cheal tissues are chronically exposed to pressure by theETT or cuff. This pressure may compress the recurrent



laryngeal nerves and cause temporary or permanent vocalcord paralysis. Likewise, when this pressure exceeds cap-illary pressure, necrosis, ulceration, and scarring may de-velop in the subglottis and trachea, leading to the forma-tion of stenosis. Comorbidities and reflux also appear toplay a role in the pathogenesis of laryngotracheal stenosis.

Airway management with video laryngoscopes such asthe GlideScope may provide better visualization duringdifficult intubation. However, several recent reports havedocumented oropharyngeal injury during tube insertion.The most accepted mechanism of injury is blind insertionof the tube by providers who are looking at the GlideScopemonitor until the ETT finally comes into view.

The supraglottic airway device is considered a less in-vasive alternative to endotracheal intubation, but its usealso has been associated with soft tissue oral cavity inju-ries and neuropraxic injury of the recurrent laryngeal, lin-gual, and hypoglossal nerves. These injuries are believedto be secondary to elevated cuff pressures against the softtissues of the oral cavity, oropharynx, and hypopharynx.

As the situations leading to airway injury during endo-tracheal intubation are understood, several key points mightaid in the prevention of complications:

• Whenever possible, recruit a second provider to assistduring difficult or emergent intubations.

• Seek early otolaryngology evaluation for patients withsevere acute soft tissue injuries, for those with severesymptoms after extubation, and for those whose symp-toms (hoarseness, dysphagia, aspiration) persist beyond1 month after extubation.

• Consider patients with comorbid conditions at higherrisk of long-term airway complications and manage ac-cordingly.

• Monitor cuff pressures and, whenever possible, limitprolonged intubation, as these may lead to vocal cordparalysis or laryngotracheal stenosis.

• For video laryngoscope intubations, directly visualizethe ETT within the oral cavity until the tip of the ETTcan be viewed on the video monitor.

• Choose a supraglottic airway device that is adequatelysized for the patient and monitor cuff pressures.

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Discussion

Durbin: We’ve just gotten in the rou-tine of measuring cuff pressures inETTs [endotracheal tubes] in the OR[operating room]. One of our residentsdid a study and found that the pres-sures were all over the place. We’vereally focused, and we have cuff pres-sure manometers on all the anesthesiamachines. Our electronic record alsosupports this, and we have to checkoff that we did measure cuff pressureand how we did it. There’s also a placeto record cuff pressure if you placedan LMA [laryngeal mask airway]. Iremember the days when we had high-pressure low-volume ETT cuffs (redrubber tubes), and the pressure in thecuff had nothing to do with the lateralwall pressure in the trachea. Now,we’re saying the pressure in the LMAcuff has something to do with the pres-sure in the pharyngeal soft tissue struc-ture? I find that hard to understandand even harder to defend. With thehigh-pressure cuff of the LMA, thepressure really is intercuff pressure,not transmural or across the tissuesoutside of the cuff. We had to put sen-sors in the trachea to actually demon-

strate that cuff pressure and mucosalpressure were not the same with high-pressure low-volume ETT cuffs.Would you comment on that regard-ing the LMA cuff pressure?

Berkow: The problem is that whatwe really think matters is tissue per-fusion, and we don’t know. Some pa-tients may be at higher risk of devel-oping injury because they have poortissue perfusion. But measuring a cuffpressure tells you what that pressureis, but it doesn’t tell you what’s hap-pening to the tissue. Since we don’tknow what the threshold is abovewhich that tissue won’t get perfused,that’s really still the unanswered ques-tion. There have been cases of patientswho were young and healthy, every-thing done right, and they still devel-oped an injury. And then other pa-tients who are extremely high risk andwere intubated for many days do fine.So, the problem is that we don’t knowhow to measure the tissue pressuresthat are really important.

Durbin: It may be the device itselfand the pressure contact places on theback or side of it causing injury. Cer-

tainly with older ETTs, the plac-eswhere they rubbed and pressed onthe larynx was more important thanthe cuff pressures were for these long-term injuries or even for short-terminjuries. I think we’ve got a long wayto go before we can say a cuff pres-sure of 40 or 60 in an LMA is a prob-lem. It may be; I don’t know. If I canget a seal with less, that seems okay tome. If I need a seal, I think allowing ahigher pressure is probably better thangiving less and risking aspiration orventilation failure.

Berkow: The other issue is that thenerves that innervate the larynx andpharynx have a huge amount of vari-ability as far as where they sit, so younever know whether you’re potentiallystretching or compressing a nerve withyour tube or LMA because you don’tknow for sure where it actually sits.There’s so much variation, so that’sstill an unknown as well.

Blank: I appreciated your thoughtson the safe use of video laryngoscopes,particularly with regard to tube inser-tion, but I wonder if you have anythoughts about the role of different



stylets? The proprietary stylet for theGlideScope, for example, is quite rigid.Would a less stiff, malleable stylet besafer?

Berkow: Yes, I didn’t include thatin my talk, but because of the moreacute angle at which you have to in-sert ETTs with the video laryngo-scopes, it’s recommended that you usethese rigid stylets, which are angled tomatch the curve of the blade. They aremuch more rigid than some of the mal-leable stylets. Certainly, that increasesyour risk of potential injury becauseyou’re putting something sharper intothe airway. That’s one of the reasonsfor recommending trying to stay mid-line and hugging the laryngoscope de-vice to keep the rigid stylet away fromthe lateral tissues. Now, I know thereare studies1,2 looking at the use of reg-ular stylets versus these proprietarystylets, and they found no differencein the rate of success, so I don’t thinkyou absolutely need to use the propri-etary stylet if you use proper tech-nique. If you use proper technique andyou get an ideal view, you should havea fairly easy passage of the tube, evenif it you are not using the rigid stylet.

Hagberg: We talk about the differ-ent generations of LMAs or SADs [su-praglottic airway devices]. Have youseen anything showing a difference incomplications with the different typesand generations of devices? Also, thedifferent categories: some are morelike the LMA, and some are more likethe combitube.

Berkow: There’s not a huge amountof literature looking at things otherthan sore throat with SADs. The moreserious injuries are just case reports,and there aren’t that many. I’m notaware of any literature that says anyone particular device is any higher riskthan another because it really dependson your cuff pressure, and you cangenerate fairly high cuff pressures withany of those devices, especially if youchoose the wrong size.

Hagberg: I know the earlier studieswith combitubes were performed incadavers, and they found little tears inthe esophageal inlet, but I’m not sureabout the laryngeal tube, and I per-sonally have not seen anything likethat.

Berkow: Right, they’re all small casereports. There’s really no large seriesof severe complications with any ofthe SADs or the video laryngoscopesat this point. They’re all individualcase reports. I guess they don’t get alot of attention; it’s not exciting topublish compared with other thingspeople are looking at.

Collins: We have a subset of patientsin the ENT [otolaryngology] popula-tion who have had previous injury, par-ticularly vocal cord injury, requiringvocal cord medialization procedures.Aside from not intubating these pa-tients for future procedures if possi-ble, or downsizing an endotrachealtube if intubation is chosen, have therebeenanyothermeasures that havebeenlooked at or assessed? Do you haveany comments about what we can ad-ditionally do for those patients?

Berkow: Certainly patients who al-ready come with an injury are poten-tially at higher risk. By definition,they’re high risk to begin with, espe-cially if they have some specific se-quelae that lead to their injury. Cer-tainly if you have someone with vocalcord paralysis, and they have a me-dian cord paralysis, potentially puttingin a smaller tube can help. There’sbeen debate about whether using anSAD or something that you don’t haveto put through the glottis itself may bebeneficial, but again, the risk of sorethroat is still fairly high with an SAD.There’s still the potential risk that ifyou stretch a nerve, you could stillhave injury; there are pros and conswith each choice. I think you just haveto have an extra level of vigilance andtry to avoid manipulating the airwayunless you absolutely have to. Many

of my ENT colleagues have said thatif you have a unilateral paralysis, theappropriately sized tube for a shortperiod time shouldn’t make that pa-ralysis any worse. If the injury’s there,if it’s permanent, it’s not going to getany better or worse from an acuteshort-term intubation. There’s not alot of literature out there about differ-ent management for patients who al-ready have injury, other than using anappropriately sized tube, shortest du-ration of intubation possible, and vig-ilance in care.

Hagberg: I think one thing we re-ally need to make sure to hone in on ismultiple intubation attempts, multipleplacement attempts of SADs: anythingwe can do in our practice in order tominimize these types of complications.The best we can do is good techniqueand not doing the same thing over andover again hoping for better results. Ifthere is failure with a type of device,it may be best to switch to an alterna-tive technique.

Berkow: I totally agree. Almost any-thing you put into the airway is harderand stiffer than the tissue of the air-way. Certainly the more things youput in and the more times you put itin, the higher risk you have for poten-tially injuring the soft tissue.

Durbin: I noticed a slide where youhad the Airtraq device, which has achannel in it and the mirror at the end.I was wondering: these devices werenot particularly popular when they firstcame out. They were disposable, butthey were $100 a piece. Our emer-gency roomphysicians and techniciansliked them, but no one else seemed towant to use them. I understand thatthey now have a non-disposable de-vice, so you could probably afford touse it. I liked the fact that the devicehas a channel for the tube, so you’renot blindly moving the ETT around inthe upper airway. We’ve pretty muchadopted the GlideScope approach, butis it time to revisit the Airtraq and



similar devices with a dedicated ETTchannel?

Berkow: There are several video la-ryngoscopes that have built-in chan-nels: there’s the Airtraq, there’s theKing Vision scope that actually offersyou the option of a channeled or un-channeled blade, and then there’s thePentax. The advantage of the channelis that the tube slides alongside thevideo laryngoscope, so there is poten-tially less risk of injury, althoughthere’s still a blind spot until it comesout. The potential disadvantage that’sbeen discussed about these channeledblades is that you have less freedomof how you introduce the tube. If thetube doesn’t go where it’s supposedto go, there’s no option to manipulatethe tube to get it in place. That’s thepotential disadvantage of a channeled

device, but certainly it should decreasethe risk of injury to the lateral struc-tures you can’t see.

Hagberg: The channeled devicesalso protect the tube, so what you’llend up finding in a truly difficult air-way is that at least you don’t have acuff tear after you finally get the tubein place. That’s one of the more pro-tective things about those devices, butI don’t think there’s a good study thatdifferentiates between channeled ver-sus non-channeled in terms of com-plication rates. It would be interestingto see.

Berkow: No, there are no studies yet.Again, the case reports on complica-tions with any of these devices havejust been coming out in the last 5 y orso. We’re not there yet. Hopefully,

someone out there is doing a study.The complications are still fairly low,so I think it’s going to be difficult toget a large trial of channeled versusunchanneled blades to look for injury.You’d have to do many patients to getenough injuries to compare signifi-cance. That’s one of the challenges.

REFERENCES

1. Sakles JC, Kalin L. The effect of styletchoice on the success rate of intubation us-ing the GlideScope video laryngoscopy inthe emergency department. Acad EmergMed 2012;19(2):235-238.

2. Turkstra TP, Harle CC, Armstrong KP,Armstrong PM, Cherry RA, Hoogstra J,Jones PM. The GlideScope-specific rigidstylet and standard malleable stylet areequally effective for GlideScope use. Can JAnaesth 2007;54(11):891-896.



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